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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 徐立中(Li-Chung Hsu) | |
| dc.contributor.author | Yu-Hsin Hsieh | en |
| dc.contributor.author | 謝佑鑫 | zh_TW |
| dc.date.accessioned | 2021-06-15T16:27:40Z | - |
| dc.date.available | 2020-09-25 | |
| dc.date.copyright | 2015-09-25 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-08-14 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/52788 | - |
| dc.description.abstract | 先天性免疫(innate immunity) 是宿主抵抗外來病原體侵略的第一道防線。Toll-like receptors (TLRs) 透過辨識pathogen-associated molecular patterns (PAMPs) 引發下游訊息傳遞,並誘發前發炎細胞激素(pro-inflammatory cytokines)以及第一型干擾素(type I interferon)的產生。TLR4訊息傳遞透過MyD88-IKKα/β-NF-κB以及TRIF- TBK1-IRF3/7途徑，分別參與在前發炎細胞激素以及第一型干擾素的生成。然而，先前研究NF- | zh_TW |
| dc.description.abstract | Toll-like receptors (TLRs) belongs to the pattern-recognition-receptors (PRRs) that sense a variety of pathogen-associated molecular patterns (PAMPs) derived from microbes to initiate the first line of host defense against invading pathogens. TLR4 engagement mediates activation of downstream MyD88-IKK-NF-κB and TRIF-TBK1-IRF3 signaling pathways leading to pro-inflammatory cytokines and type I interferon production, respectively. We previously found that TBK1 deficiency resulted in defective production of certain NF- | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T16:27:40Z (GMT). No. of bitstreams: 1 ntu-104-R02448004-1.pdf: 3599255 bytes, checksum: e495a29aef37e6c7edf667bdf88f3b9f (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | 口試委員會審定書 i 致謝 ii 摘要 iii Abstract iv Contents 1 Introduction 5 Toll-like Receptors 7 MyD88-dependent signaling pathway 9 TRIF-dependent signaling pathway 10 TRIF-dependent late phase NF-kB activation 12 TBK1 activation and its roles in innate immune signaling 13 SUMO machinery: mechanism and its role in innate immune 15 Specific aims 17 Materials and Methods 18 Antibodies and Reagents List 18 Plasmids List 19 Cell line, Cell culture and Transfection 20 Lentiviral infaction and shRNA-Mediated Gene Silencing 20 Preparation of total cell lysate 21 Immunoblotting 22 Immunoprecipitation 22 Preparation of nuclear and cytosolic extracts 23 Enzyme-linked immunosorbent assay (ELISA) 24 RNA extraction and Quantitative RT-PCR (RT-qPCR) 25 Electroporation 26 CRISPR/Cas9-mediated depletion of TBK1 in RAW264.7 murine macrophages 26 Statistical analysis 27 Results 28 TBK1 is required for p65 phosphorylation at Ser536 but not nuclear translocation upon LPS treatment 28 Generation of TBK1-/- RAW264.7 macrophages using CRISPR/Cas9 system 29 TBK1 deficiency diminishes the expression of both type I interferon and NF-κB-mediated proinflammatory cytokines in LPS- and poly(I:C)-stimulated RAW264.7 macrophages. 30 TBK1 is modified by SUMO1 conjugation upon poly(I:C) treatment. 31 TBK1 SUMOylation is not required for TBK1 activation. 31 TBK1 SUMOylation is critical for the production of pro-inflammatory cytokines upon LPS stimulation. 33 Discussion 34 The role of TBK1 in modulating NF-κB activity 36 Subcellular localization of TBK1 controls downstream signal responses 37 Post-translational modification defines the functional consequences of TBK1 38 The E3 ligase catalyzed TBK1 SUMOylation remains obscure. 40 Figures 43 Figure. 1 TBK1 is necessary for LPS-induced p65 Ser536 phosphorylation without impairing IKK | |
| dc.language.iso | en | |
| dc.subject | TLR訊息傳遞 | zh_TW |
| dc.subject | 小泛素化 | zh_TW |
| dc.subject | TLR signaling pathway | en |
| dc.subject | SUMOylation | en |
| dc.title | TBK1小泛素化在TLR3/4訊號傳遞所扮演之功能角色 | zh_TW |
| dc.title | The functional role of TBK1 SUMOylation in TLR3/4 signaling pathway | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 林琬琬(Wan-Wan Lin),劉旻禕(Helene Minyi Liu) | |
| dc.subject.keyword | TLR訊息傳遞,小泛素化, | zh_TW |
| dc.subject.keyword | TLR signaling pathway,SUMOylation, | en |
| dc.relation.page | 69 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2015-08-14 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
| 顯示於系所單位： | 分子醫學研究所 | |
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